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Psychosomatic Medicine 65:938-943 (2003)
© 2003 American Psychosomatic Society

ORIGINAL ARTICLES

Effect on Disability Outcomes of a Depression Relapse Prevention Program

Michael Von Korff, ScD, Wayne Katon, MD, Carolyn Rutter, PhD, Evette Ludman, PhD, Greg Simon, MD, MPH, Elizabeth Lin, MD, MPH and Terry Bush, PhD

Center for Health Studies (M.V.K., C.R., E.L., G.S., E.L., T.B.), Group Health Cooperative, Seattle, WA and Department of Psychiatry and Behavioral Sciences (W.K.), University of Washington.

Address correspondence and reprint requests to Michael Von Korff, ScDPh, Center for Health Studies, Group Health Cooperative, 1730 Minor Avenue, Suite 1600, Seattle, WA 98101206-287-2874. E-mail: Vonkorff.M{at}GHC.ORG


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
OBJECTIVE: This report evaluates the effects of a depression relapse prevention program on disability outcomes among patients treated for depression at high risk for relapse.

MATERIALS AND METHODS: Primary care patients initiating antidepressant treatment for depression were assessed 6 to 8 weeks after the initial prescription. Patients responding to initial treatment but at high risk for relapse were randomized to usual care or a relapse prevention intervention (N= 386). The 12-month relapse prevention program included systematic patient education, two psycho-educational visits with a depression prevention specialist, shared decision-making regarding maintenance pharmacotherapy, and ongoing monitoring of medication adherence and depressive symptoms via telephone and mail. Disability outcomes were assessed via blinded telephone assessments at 3, 6, 9, and 12 months using SF-36 and Sheehan Disability scales.

RESULTS: Usual care patients and relapse prevention program patients had high rates of use of maintenance pharmacotherapy. Both relapse prevention and usual care patients showed improved functioning over the 12-month follow-up period. One of the three disability measures (the SF-36 Social Function scale) showed a significant intervention effect because of continuing improvement at 9 and 12 month follow-up, whereas the Sheehan Disability Scale showed a nonsignificant trend toward greater improvements in disability among relapse prevention patients than among usual care controls.

CONCLUSIONS: Moderate effects of a relapse prevention intervention on depressive symptoms were associated with modest and variable effects on disability outcomes. Inconsistent effects of the intervention for disability outcomes may be because of the high rates of maintenance pharmacotherapy among usual care patients, relatively mild levels of depressive symptoms among both intervention and control patients at baseline, the absence of a specific relapse prevention effect of the intervention, and the resultant modest differences in depressive symptoms between intervention and control patients in this trial.

Key Words: depression, • disability, • randomized trial, • relapse prevention.

Abbreviations: GHC = Group Health Cooperative;; SCID = Structured Clinical Interview for DSM-IV.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Depressive illness has been shown to be associated with significant social role disability in a wide range of populations (1–3). The levels of disability among depressed patients are as great as or greater than among patients with major physical diseases (1). Disability improves significantly as depression improves while chronically depressed patients often experience poor disability outcomes (4, 5).

A series of randomized controlled trials has now shown that enhanced care of major depression in the primary care setting can improve disability outcomes (6–10). Recently, Wells et al. reported that enhanced care of major depression increased retention in employment at 1-year follow-up (10). However, a few trials of enhanced depression care have not found improved disability outcomes even though some improvement in symptoms was reported (11,12). These negative results may be because of use of disability measures that are insensitive to change in functional status in nongeriatric depressed populations (eg, the SF-12 physical function scale) and to small effect sizes for depressive symptom outcomes caused by significant numbers of usual care patients who were adequately treated. Overall, experimental studies now support a conclusion that enhanced acute phase treatment of major depression in the primary care setting improves disability outcomes.

Among primary care patients with major depression, recurrences are common (13). Sustained treatment of severely depressed patients in continuation and maintenance phases after effective acute phase treatment has been shown to reduce relapse rates (14–17). However, little is known about the effects of sustained treatment on disability outcomes, particularly among the less severely depressed patients treated in primary care settings.

In earlier articles, we described a relapse prevention program for primary care patients recovered from a depressive episode who remained at high risk for relapse (18). This relapse prevention program improved medication adherence and resulted in modest improvements in depressive symptoms at 9- and 12-month follow-up relative to a care as usual control group (19,20). The objective of this article is to assess the effects of this program on disability outcomes.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
The intervention, methods, and effects on depression outcomes of this study are fully reported in previous articles (18–20). Participants were recruited from four large primary care clinics of Group Health Cooperative (GHC), a group model health maintenance organization serving approximately 400,000 persons in Washington State. Computerized pharmacy and visit registration records were used to identify all patients receiving a new antidepressant prescription from a primary care physician associated with a visit diagnosis of a depressive disorder (including physician diagnoses of major depressive episode, dysthymia, and depressive disorder NOS). A "new" prescription was defined by an interval of at least 120 days since last use of an antidepressant (based on prescription date and intended duration of use). An invitation letter was mailed to all potentially eligible patients approximately 1 month after the initial prescription. Potential participants were then contacted by telephone 6 to 8 weeks after the initial prescription. After a documented oral consent procedure, participants completed a telephone screening assessment including the current and past depression modules of the Structured Clinical Interview for DSM-IV (or SCID) (21). Patients were invited to participate in an in-person baseline assessment based on the following criteria: significant residual symptoms (ie, four or more of the nine DSM-IV depression criteria), current dysthymia (ie, depressive symptoms present for 2 years or more), or history of recurrent depression (ie, 2 or more previous depressive episodes). The baseline assessment typically occurred approximately 2 months after the primary care visit that initiated depression treatment. The in-person baseline assessment included a 20-item depression scale extracted from the SCL-90 (22). Clinical eligibility criteria included remission of the index depressive episode (defined as either less than four of the nine DSM-IV depression criteria or four DSM-IV depression criteria with SCL depression score less than 1.0) and high risk for relapse (defined as a history of 3 or more lifetime depressive episodes or a history of dysthymic disorder). Criteria for exclusion were: score of 2 or more on the CAGE alcohol questionnaire, plans to disenroll from GHC within 12 months, recent use of mood stabilizer or antipsychotic medication, pregnant or nursing, and current medication management by a psychiatrist. After a full explanation of study procedures, written informed consent was obtained from all participants.

Patients assigned to the usual care group could receive any services normally available inside or outside of GHC—including referral to specialty mental health care. No additional services were provided, but no services usually available were limited or withheld.

The relapse prevention program (18) was a multifaceted intervention including the following components: (1) an educational book and videotape regarding effective management of depression, with a focus on chronic or recurrent depression; (2) two in-person visits with a depression prevention specialist, including shared decision-making regarding maintenance antidepressant treatment; (3) three scheduled telephone monitoring contacts (2, 5, and 9 months after enrollment) including monitoring of depressive symptoms and treatment adherence; and (4) four personalized mailings (3, 6, 10, and 12 months after enrollment) for continued monitoring of depressive symptoms and treatment adherence.

Depression prevention specialists communicated regularly with treating primary care physicians regarding treatment discontinuation, signs of depressive relapse, or other situations requiring clinical attention (eg, intolerable medication side effects). Treating primary care clinicians remained responsible for all pharmacotherapy decisions. If needed, patients were referred for in-person consultation with an on-site liaison psychiatrist or for ongoing treatment in GHC’s specialty behavioral health clinic. Each depression prevention specialist met with a supervising psychiatrist (in-person or by telephone) for 15 to 30 minutes each week.

The baseline interview occurred immediately before randomization. Clinical outcomes were subsequently assessed via blinded telephone interviews 3, 6, 9, and 12 months after randomization. These interviews included repeat administration of the SCL-90 depression scale (the primary outcome measure). Disability outcomes were measured by the Sheehan Disability Scale (23) and by the SF-36 social function and role emotional scales (24). The Sheehan Disability Scale consists of three 0 to 10 ratings of the extent that illness interferences with work, family, and social life. The SF-36 social function scale asks patients to rate the degree to which physical health or emotional problems interfered with social activities with family, friends, neighbors, or groups, and the amount of time physical health or emotional problems interfered with social activities like visiting with friends and close relatives. The role emotional scale asks about the amount of time the patient: decreased work and other activities because of emotional problems; accomplished less than they would like; and performed work or other activities less carefully than usual.

We assessed the effect of time and intervention on disability outcomes using linear regression models. The regression models were used to estimate the effect of treatment while adjusting for age, sex, physical co-morbidity [Chronic Disease Score (25, 26) ], neuroticism (NEO) (27), and baseline SCL score. These models accounted for correlation in longitudinal assessments across the four follow-up times using an unstructured correlation matrix, with estimation performed using generalized estimating equations. The regression models included an overall effect of intervention, a linear time effect, and an interaction between time and intervention (28–30).

We found differences in follow-up rates for intervention and usual care groups, with somewhat higher rates of follow-up among intervention than usual care patients. Across all interviews, 10.1% of follow-up interviews were missing: 6.2% in the intervention group and 12.5% in the control group. The proportion of interviews that were missing increased over the follow-up period, with 10.3% of the intervention group and 20.8% of the usual care group missing interviews at 12 months. We assumed that missing data depended only on observed outcomes and used observed data to account for differential drop-out via multiple imputation with propensity-score matching of missing to observed cases (31). We adjusted only for unit nonresponse (ie, missing interviews) because there was very little item nonresponse. Propensity scores were estimated separately for each time point using logistic regression models with completely observed baseline covariates (randomization group, married, live alone, single parent, college graduate, panic attack in the past 2 weeks, self-rated health, self-reported high stress, satisfaction with HMO care, physical co-morbidity (CDS), and baseline SCL). Propensity score matching was stratified by intervention group, quartile of propensity score, and interview. We imputed data for entire cases, but separately for each missed follow-up time, thereby incorporating the cross-sectional correlation of outcome and covariate data, but ignoring between time correlation of outcomes. Probabilities of nonresponse based on this set of variables achieved good prediction of nonresponse status at each follow-up. For example, at the 12 month follow-up, the estimated probability of nonresponse exceeded 25% for 13% of subjects actually interviewed versus 40% of subjects who were missing. We report analyses for both the observed data and the observed data augmented with imputed values for persons with missing observations at follow-up. The observed and missing results were quite similar for disability outcomes.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
In the study participation, a total of 386 patients were enrolled in the randomized trial (194 assigned to the relapse prevention program and 192 to usual care). Of this number, 315 (82%) completed all blinded follow-up assessments and 377 (98%) remained enrolled in GHC throughout the follow-up period. The proportion of patients completing all follow- up assessments was 88% (170/194) in the intervention group compared with 76% (145/192) in the usual care group (2 = 9.43, p= 0.002). Those completing all follow-up assessments also had significantly lower SCL depression scores at baseline (mean 0.82, SD 0.36 vs. mean 0.92, SD 0.38; t = 2.15, df= 384, p= 0.03). Participation in blinded follow-up assessments was not significantly associated with age or sex.

Across the 14 variables examined, there was only one significant difference in participant characteristics between the intervention and control groups. Usual care patients were somewhat more likely to have met criteria for major depression within the previous year (Table 1). The baseline SCL score in both the intervention and control groups was approximately 0.84, indicating mild depressive symptoms as an SCL score of 0.5 or less indicates remission. While patients enrolled in this relapse prevention trial were substantially improved subsequent to treatment, and none met criteria for current major depression, the typical study participant continued to have mild to moderate depressive symptoms. Three-quarters had a previous history of three or more depressive episodes, and approximately half had a history of dysthymia. Thus, the enrolled patients typically had a history of recurrent or chronic depression, and most continued to have mild depressive symptoms when enrolled. More than 80% were on antidepressant medication at the outset of the study.


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  		TABLE 1. Demographic and Clinical Characteristics of Depressed Patients
 
As reported previously (19), the proportion of usual care patients continuing antidepressant medication in the 9- to 12-month follow-up period was 50% in the usual care group compared with 63% in the intervention group. In the usual care group, the mean SCL score was 0.84 (SD = 0.35) at baseline, 0.79 (0.47) at 3 months, 0.78 (0.51) at 6 months, 0.86 (0.57) at 9 months, and 0.74 (0.54) at 12 months. In contrast, in the intervention group, the mean SCL score decreased from 0.83 (SD = 0.39) at baseline to 0.75 (0.55) at 3 months, 0.74 (0.54) at 6 months, 0.69 (0.56) at 9 months, and 0.65 (0.51) at 12 months. Across the 12-month follow-up period, mean SCL depression score was somewhat lower in the intervention group (mean difference = 0.08, p= 0.04).

As shown in Figure 1 and Table 2, intervention patients showed more favorable outcomes for the SF-36 Social Function scale than did usual care patients. Note that a higher score on this scale indicates lower levels of disability. The two groups showed equal improvement in disability from baseline to 6 months. After 6 months, the intervention group showed further improvements in social function scores, whereas the usual care controls showed no additional improvement in disability status on this measure after 6 months. After controlling for covariates, the time by intervention effect was statistically significant (p< 0.05).



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  		Figure 1. SF-36 Social Function outcomes for relapse prevention program (RPP) patients compared with usual care control group patients (observed data without imputation).

 

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  		TABLE 2. SF-36 Social Function
 
The results for the role emotional scale of the SF-36 were similar in one respect and different in another. Both intervention and usual care patients showed improvements in disability status over time (p< 0.01), after controlling for covariates (Table 3). However, intervention patients did not show significantly better disability outcomes than usual care patients on this scale as assessed by the time by intervention interaction term (p= 0.78).


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  		TABLE 3. SF-36 Role—Emotional
 
For the Sheehan Disability Scale, both intervention and usual care patients tended to show improvement in disability over time (Table 4). While the time by intervention interaction effect was nonsignificant (p= 0.14), the intervention patients tended to show greater improvements in disability on this measure than patients receiving care as usual.


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  		TABLE 4. Sheehan Disability Score
 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
ACKNOWLEDGMENTS
 REFERENCES
 
This study assessed whether a low-intensity relapse prevention program resulted in better disability outcomes than Usual Care. The results for disability outcomes were mixed. One of three disability measures (the SF-36 Social Function scale) showed a significant intervention effect due to continuing improvement at 9 and 12 month follow-up, while the Sheehan Disability Scale showed a nonsignificant trend toward greater improvements in disability among relapse prevention patients than among usual care controls.

Both the intervention and control group patients had, on average, only moderate levels of depressive symptoms at baseline, leaving only limited room for subsequent improvement in depressive symptom levels. The most severely depressed primary care patients, those who continued to have moderate to severe depressive symptoms when screened for enrollment, were not eligible for this relapse prevention study. In addition, a large percentage of the usual care patients continued to receive antidepressant treatment at long-term follow-up. Because many control patients continued to use antidepressant medication, the observed effect of the relapse prevention intervention on depressive symptoms may have been mitigated relative to a design in which the control group received no treatment or a placebo. While the intervention did produce a modest beneficial effect on depressive symptoms, the intervention did not result in a difference in relapse rates over the 1-year follow-up period. We believe the variable and modest effects on disability outcomes reflect the modest effects on depressive symptoms. In previous acute depression treatment trials, the magnitude of the effect on disability outcomes has been in proportion to the magnitude of the effect on depressive symptoms. In this trial, the lack of a relapse prevention effect, the low baseline levels of depressive symptoms, and the higher than expected rates of long-term antidepressant therapy in the usual care control group appear to have resulted in both a modest effect on depressive symptoms and a correspondingly modest and variable effect on disability outcomes. In previous acute phase depression treatment trials, effect sizes for disability outcomes have tended to be smaller than effects sizes for depressive symptom outcomes. In light of the modest effect of the intervention on depressive symptoms, the results for disability outcomes appear to be in keeping with the results of previous intervention trials, which have also reported mixed results for disability outcomes across trials and measures.

Our results suggest avenues for future research on the effects of relapse prevention interventions on disability outcomes. It is important to note that the effect of the intervention was through enhancing control of depressive symptoms rather than through prevention of relapse per se. If active follow-up support were targeted to patients unlikely to continue antidepressant treatment, then effects of the intervention on depression and disability outcomes might be greater. Similarly, targeting patients with moderate to severe residual symptoms, as opposed to the patients enrolled in this study with generally mild depressive symptoms, might increase the magnitude of the effect of a relapse prevention intervention relative to care as usual.

Because disability outcomes continued to show improvement over the 1-year follow-up for both intervention and control patients, it suggests that recovery from a major depressive episode in this population of patients at high risk for relapse is a gradual process. Approximately one-third of the intervention and control patients experienced a major depressive episode during the 1-year follow-up (19), although these episodes were typically brief. The intervention tested here did not reduce the frequency of these recurrences, perhaps because of the patient population targeted, the intensity of the intervention, and/or the high rates of antidepressant treatment in the usual care control group. There is a need for practical approaches to active follow-up of high-risk patients recovering from major depressive episode that can prevent relapse, achieve optimal control of residual symptoms, and thereby achieve maximal restoration of functioning in work, family, and social life. The results of this study suggest that further research is needed on effective ways of targeting and sustaining treatment for depressed patients at high risk for relapse.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
This research was supported by NIH grant MH41739 from the National Institute of Mental Health.

Received for publication April 25, 2003.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

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